The major avenues of investigation in progress are: (1) Enhancement of flavin synthesis in newborn rats by maternal riboflavin deficiency. After administration of C14-riboflavin to newborn rats, rates of incorporation of isotope into C14-FMN and C14-FAD in liver and brain were increased 2-fold in progeny of riboflavin deficient rats. (2) Regulation of L-triiodothyronine aminotransferase activity by T3 in normal and neoplastic cells. This recently described enzyme is probably involved in the metabolic degradation of triiodothyronine (T3). Enzyme activity in Novikoff hepatoma is half that of liver of tumor-bearing rats, and in contrast to liver, is unchanged after administration of T3 in vivo. (3) Riboflavin excretion and turnover in an unusual case of multiple myeloma. An 80 year old female patient was noted to have a monoclonal IgG lambda protein in her serum that binds riboflavin with high affinity. Clinical studies with riboflavin loading in vivo demonstrated an enormous delay in the turnover and excretion of riboflavin. (4) Hormonal control of flavin metabolism. Thyroid hormones enhance FAD synthesis similarly in livers of newborn and adult rats. By contrast, thyroid hormones increase FAD synthesis in brains of newborn but not adult animals. (5) Experimental approaches to the pathogenesis of cancer-induced cachexia. Transplants of Novikoff hepatoma in the peritoneal cavity of normal animals consistently exhibit rapid rates of flavin synthesis. Studies are in progress determining the effects of riboflavin deficiency upon flavin synthesis in tumor and in host liver. BIBLIOGRAPHIC REFERENCES: Riboflavin. Rivlin, R.S., ed. New York, Plenum Press, 1975, 433 pages. (Chapters by R.S. Rivlin: (1) Preface, (2) Riboflavin and Cancer, (3) Hormonal Control of Riboflavin Metabolism). Sturman, J., and Rivlin, R.S. Pathogenesis of brain dysfunction in deficiencies of thiamine, pantothenic acid, riboflavin and pyridoxine. In: Biology of Brain Dysfunction, G.E. Gaull, ed. (New York: Plenum Press, 1975), pp. 425-475.